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10.1158/0008-5472.CAN-16-0401 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-16-0401 C5082982!5082982!27261507     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27261507&cmd=llinks): Failed to open stream: HTTP request failed! 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Definition of a novel feed-forward mechanism for glycolysis-HIF1? signaling in hypoxic tumors highlights adolase A as a therapeutic target |pdf=|usr=}}{{27261507}} gab.com Text Definition of a novel feed-forward mechanism for glycolysis-HIF1 signaling in hypoxic tumors highlights adolase A as a therapeutic target JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27261507 #FOAvip The hypoxia-inducible transcription factor HIF1? drives expression of many glycolytic enzymes. Here we show that hypoxic glycolysis, in turn, increases HIF1? transcriptional activity and stimulates tumor growth, revealing a novel feed-forward mechanism of glycolysis-HIF1? signaling. Negative regulation of HIF1? by AMPK1 is bypassed in hypoxic cells, due to ATP elevation by increased glycolysis, thereby preventing phosphorylation and inactivation of the HIF1? transcriptional co-activator p300. Notably, of the HIF1? activated glycolytic enzymes we evaluated by gene silencing, aldolase A (ALDOA) blockade produced the most robust decrease in glycolysis, HIF-1 activity and cancer cell proliferation. Furthermore, either RNAi-mediated silencing of ALDOA or systemic treatment with a specific small molecule inhibitor of aldolase A was sufficient to increase overall survival in a xenograft model of metastatic breast cancer. In establishing a novel glycolysis-HIF-1? feed-forward mechanism in hypoxic tumor cell, our results also provide a preclinical rationale to develop aldolase A inhibitors as a generalized strategy to treat intractable hypoxic cancer cells found widely in most solid tumors. Twit Text FOAVip Definition of a novel feed-forward mechanism for glycolysis-HIF1 signaling in hypoxic tumors highlights adolase A as a therapeutic target ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27261507 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27261507 #FOAvip English Wikipedia <ref>{{Cite pmid|27261507}}</ref> Definition of a novel feed-forward mechanism for glycolysis-HIF1? signaling in hypoxic tumors highlights adolase A as a therapeutic target #MMPMID27261507 Grandjean G; De Jong P; James B; Koh MY; Lemos R; Kingston J; Aleshin A; Bankston LA; Miller CP; Cho EJ; Edupuganti R; Devkota A; Stancu G; Liddington RC; Dalby K; Powis G Cancer Res 2016[Jul]; 76 (14): 4259-69 PMID27261507show ga The hypoxia-inducible transcription factor HIF1? drives expression of many glycolytic enzymes. Here we show that hypoxic glycolysis, in turn, increases HIF1? transcriptional activity and stimulates tumor growth, revealing a novel feed-forward mechanism of glycolysis-HIF1? signaling. Negative regulation of HIF1? by AMPK1 is bypassed in hypoxic cells, due to ATP elevation by increased glycolysis, thereby preventing phosphorylation and inactivation of the HIF1? transcriptional co-activator p300. Notably, of the HIF1? activated glycolytic enzymes we evaluated by gene silencing, aldolase A (ALDOA) blockade produced the most robust decrease in glycolysis, HIF-1 activity and cancer cell proliferation. Furthermore, either RNAi-mediated silencing of ALDOA or systemic treatment with a specific small molecule inhibitor of aldolase A was sufficient to increase overall survival in a xenograft model of metastatic breast cancer. In establishing a novel glycolysis-HIF-1? feed-forward mechanism in hypoxic tumor cell, our results also provide a preclinical rationale to develop aldolase A inhibitors as a generalized strategy to treat intractable hypoxic cancer cells found widely in most solid tumors. äDefinition of a novel feed-forward mechanism for glycolysis-HIF1? sign(epmc).pdf DeepDyve Pubget Overpricing